| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Outline of Final Research Achievements |
Dysbiosis reportedly occurs in patients with obesity and type 2 diabetes. Dysbiosis is considered to induce systemic chronic inflammation and the alteration of intestinal hormone secretion. These changes cause obesity and type 2 diabetes. The mechanism of dysbiosis remains to be elucidated. We have found that modulation of intestinal bile acid metabolism in the subjects with metabolic disorders prevented dysbiosis, preserved intestinal barriers, and prevented obesity dependent on intestinal microbiota, indicating that intestinal microbiota could be therapeutic targets in patients with the diseases.
We investigated the effects of incretin on metabolic parameters, microbiota, and immune cells in various mouse models and incretin was found to alter the intestinal environment. The mechanism by which incretin altered the intestinal function would be dependent on a suppression of inflammation. The intestinal inflammation could be the important target of metabolic disorders.
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